IGF-1 serves as a priming agent for biologic functions of leukocytes.

ObjectiveTo study the effects of growth hormone (GH) and insulinlike growth factor 1 (IGF-1) on whole body and gastrointestinal (Gl), hepatic, femoral, and renal glutamine (GLN) uptake and release in septic piglets. Summary Background DataThe GI metabolism of GLN is impaired during sepsis, and this may contribute to a breakdown of the gut's mucosal barrier. GH treatment has produced increased GI GLN uptake in surgical stress. Uttle is known about the effects of GH and IGF-1 in sepsis. MethodsTwenty-four piglets were randomized to three groups of eight each: a GH group received a bolus of 16 IU of Genotropin; an IGF-1 group received a continuous infusion of 1.3 mg/hour of IGF-1; and a control group received saline. After surgical preparation, sepsis was induced with live Escherichia coli bacteria. Using isotope technique, whole body tumover and organ-specific absolute uptake and release were measured before and 4 hours after sepsis. ResuftsAfter sepsis, both GH and IGF-1 treatment increased GI GLN uptake compared with controls and induced hepatic release of GLN. GLN release from skeletal muscle was diminished in all groups after sepsis. Whole body GLN tumover was increased in the GH and IGF-1 groups compared with the controls, before and after sepsis. ConclusionsGH and IGF-1 treatment induced increased GI net uptake of GLN. GH and IGF-1 treatment also promoted absolute and net release of GLN from the liver. This release might facilitate increased GI uptake despite reduced hindleg release in the early phase of sepsis. difference between sepsis and surgical stress is the handling of GLN by the bowel. Gut uptake of circulating GLN is diminished in septic patients and in endotoxemic rats and is associated with decreased mucosal glutaminase activity.10In surgical stress, however, the uptake of circulating GLN is increased.8Growth hormone (GH) reduces skeletal muscle release of GLN in catabolic states.'11-4 Despite reduced skeletal muscle release, increased GI uptake of GLN and reduced hepatic uptake were found after pretreatment with GH in a porcine trauma model.'5"6 The combination of reduced skeletal muscle GLN release, increased GI uptake, and net hepatic release may suggest that GH improves GLN economy after surgical stress, possibly by stimulating hepatic GLN synthesis rather than ureagenesis. However, most clin-131

When given after gastrointestinal surgery in patients treated with total parenteral nutrition, growth hormone treatment abolished glutamine, 3-methylhistidine, and total amino acid nitrogen loss from forearm tissue. Alanine loss from forearm tissue was attenuated.

GH promoted metabolic acidosis in traumatized sepsis and impaired compensation of a subsequent hemorrhage.